P-Plex, M-drol or Havoc for strength only?

Which compound run SOLO, would be the best for strength gain with the least amount of weight gain. Diet will be high protein, moderate carbs and fat. Do not want to stack any of these together and strength gain is the only goal.

Diet will determine weight gain... but I know what you mean. None of those are the best options for gaining strength without gaining weight... SD and PP are reliant on a good amount of water/glycogen "temporary weight" from my experience, you could maintain weight if you work to burn the fat off.

With havoc you could accomplish what you want if you use a high dose and do proper diet/cardio to keep weight down but really i don't think it promotes weight gain as much.

I think the best PH for what you want would be Tren, a lot of people report heavy weight gain on it but I think it's well suited for gaining strength without mass.

The other thing I would consider for your requirements is a high dose of Hdrol, possibly stacked with low/moderate doses of Epi or Tren.

If you had access to AAS you'd have some better options like winstrol, anavar, well Halotestin but maybe I shouldn't mention that one :P

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Thanks for your advice. H-drol at 100 mgs for 6 weeks worked well for me, but I am wanting to try something a bit stronger. I stacked the H-drol with 800mgs of Bold and it was succesful even after PCT. I didn't think of Tren, since it is not a methyl, would stacking it with any of these three work well? Again, the more strength the better. I can deal with 8 or 9 pounds of weight gain.

In my experience m-drol would be the route to go. Most ppl retain little to no water on this compound, and the strength gains are sic. weight gain due to increase in lbm will still exist, but they should all be very dry.

i ran two solo mdrol cycles, i didn't notice anything compared to my epistane/hdrol 6 week cycle.
my bench went up about 30 lbs over the 6 wks, maybe i just ran the mdrol wrong nutrition wise..idk. im definately keeping epistane in my stacks from now on though

If you're concerned about strength only, you must consider and strength training routine and another diet.

Dude, I actually compete in powerlifting and I am trying to get my Elite total in the 275 pound weight class in the USPF. My routine is fine and my diet is fine as well. I am just looking for an advantage without ordering illegal steroids through the internet. I have these three drugs and want to know what peoples experience is with any f them run solo as it pertains to strngth without too much weight gain and bloat.

I'd stay away from the Pheraplex based upon what you seem to be looking for. I just stopped an Epistane/Pheraplex cycle early because the Pheraplex was wreaking havoc with me. I gained about 16 lbs in 4 weeks and it seems like it is mostly h20 weight. I'm puffy and bloated and that was not really what I was looking for when I decided to stack the Phera w/ Epi. With me, the Pheraplex appears to be a sopping wet designer. My back pumps were so bad from the Phera, all of my compound lifts went down and it got hard to even complete a workout.

In my experience m-drol would be the route to go. Most ppl retain little to no water on this compound, and the strength gains are sic. weight gain due to increase in lbm will still exist, but they should all be very dry.

I gain weight like mad on Superdrol though, not so much the water as the glycogen and filling of the muscles, a huge percentage of that intramuscular weight is water even if there's less water retention elsewhere. Anyway, i was eating x calories and not gaining weight, started SD, started gaining a pound a day at least. So i didn't even increase my calories and I started gaining... So I would say it's very prone to weight gain.

I do agree tho that SD is the best thing for strength out there, everytime I take Superdrol my pressing (which is my weakest area) explodes.

I think you could run SD to achieve these goals but proper diet and cardio should be done to control the weight gain. I'd still feel safer recommending an Hdrol/Tren stack as those can be ramped up to pretty high doses with excellent strength and very managable weight gain

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If you're concerned about strength only, you must consider and strength training routine and another diet.

this is right. you ask for advice then get upset when you get it. any of these will increase strength. and your diet will determine how much weight you gain/loose. again, diet is what can allow you to cut on test, or bulk up.

I feel epistane would be the easiest if you dont know how to diet well. sd stacked with pp if you do know how to diet well would be your best bet for strength.

When I ran SD on a bulk each time the first week i did 10mg and gained around 10 pounds

When I ran SD stacked with PP on a recomp, in order to maintain weight I ate 3k calories, did cardio 1x to 2x a day, and was on T3. I imagine without the ridiculous amount of cardio and the T3, and on normal maintenance calories (more like 3500) I would have gained weight stupidly fast

when weight comes on that fast, its not muscle. Its rapid uptake of water and glycogen puffing out the muscles. Its not keepable by itself, but it allows your muscles to work way harder and get way stronger, and its in the ensuing days that actual muscle is built. thought i should clarify that.

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Dude, I actually compete in powerlifting and I am trying to get my Elite total in the 275 pound weight class in the USPF. My routine is fine and my diet is fine as well. I am just looking for an advantage without ordering illegal steroids through the internet. I have these three drugs and want to know what peoples experience is with any f them run solo as it pertains to strngth without too much weight gain and bloat.

Recently there was a study performed in which subjects were overfed by 50% of their maintenance caloric needs of purely carbohydrates-all simple sugars. The results concluded that activation of de novo lipogenesis in these subjects only produced 4g of fat each day. De novo lipogenesis is not very active and responsive in humans, it is however very active in other mammalian species. I can't find the article for this study, but here is another one I have.

DISCUSSION

We compared the response of liver and adipose tissue lipogenesis to acute and chronic stimulation by carbohydrate ingestion. Hepatic lipogenesis was, in agreement with previous studies (7, 8, 31) clearly responsive to both acute and chronic stimulation while adipose tissue DNL appeared on the contrary poorly responsive. This conclusion is based on several lines of
evidence. First, although oral glucose ingestion in study 2 prevented the decrease in both FAS and SREBP1c mRNA concentrations observed in study 1 there was no increase in these concentrations, as well as in ACC1 mRNA value. This strongly suggests that the expression of lipogenic genes, and presumably the activity of the corresponding proteins, were only
minimally stimulated in adipose tissue by the 12 hour rise in plasma insulin and glucose.

Measurements of proteins amounts and enzyme activity were precluded by the small amount of adipose tissue obtained by needle biopsy. However, there is no shortterm regulation of FAS activity and changes in activity are linked to changes in mRNA level (32). With respect to SREBP1c, the present evidence is that its main regulation is at the transcriptional level and that its activation by proteolytic cleavage is probably a constitutive, nonregulated process (33). The present in vivo result contrasts with in vitro studies showing a stimulation of FAS expression and activity by insulin in human adipocytes (12). Second, FAS, ACC1 and SREBP1c mRNA levels were not increased, but rather decreased, during the high energy high carboydrate diet suggesting strongly that the lipogenic pathway was not stimulated in adipose tissue by carbohydrate overfeeding. Third, these results are consistent with the tracer14 derived estimates of adipose tissue lipogenesis we obtained. The comparaison of deuteriumband 13C enrichments in plasma and adipose tissue TAG clearly shows that adipose tissue lipogenesis was active under the three situations studied. The lack of detectable enrichment in 13C of adipose TAG does not exclude that some uptake of TAGFA occured but shows that this uptake, if present, is low and does not contribute to the deuterium enrichment measured inbadipose TAG. There was, however, no stimulation of lipogenesis in adipose tissue by acute glucose oral load and only a non significant trend for higher lipogenic rate after chronic carbohydrate overfeeding. As a result adipose tissue lipogenesis which was quantitatively comparable to liver lipogenesis in the absence of stimulation (study 1) became less important during either acute or chronic stimulation by carbohydrate feeding. Overall our results agree with those of previous studies which used the incorpation in adipose tissue lipids of 14C from glucose to estimate lipogenesis (4, 5, 15, 34).

We think thus that the stimulation of adipose tissue lipogenesis by massive carbohydrate overfeeding suggested by the study of Aarsland et al (8) is, if real, present only during such extreme, unphysiological situation. The regulation of adipose tissue lipogenesis appears thus different in human beings compared with some other mammalian species. In rats for example adipose tissue lipogenesis is more active and is, as liver lipogenesis, responsive to high insulin/glucose levels and to variations of carbohydrate intake (35, 36). SREBP1c plays a major role in the regulation of lipogenic genes expression, at least in their response to insulin (18, 37, 38). This transcription factor is a major determinant of the lipogenic capacity of mammalian and avian tissues (39). Therefore it is possible that SREBP1c expression is low in human adipose tissue, compared to other species, but such comparison between human beings and other species has not been performed to our knowledge. The lack of response in our study of adipose tissue FAS and ACC1 expression and lipogenesis to acute or chronic carbohydrates overfeeding could be related to the lack of increase of SREBP1c mRNA. Since SREBP1c expression is stimulated in rats by dietary carbohydrates and/or insulin (18, 40, 41) it would remain to determine why this stimulation is absent in human adipose tissue.

The comparison of the quantitative estimate of hepatic and adipose lipogenesis during study 2 with the amount of glucose ingested (less than 1g vs 250270g) shows that the
contribution of this metabolic pathway to the disposal of ingested glucose was minimal. The increase of hepatic and adipose lipogenesis after an hypercaloric high carbohydrate diet (11.5 g/day) was also moderate and can thus explain only a minimal part the weight gain of the
subjects (1500g in average during the two weeks of controled diet). Since liver biopsies for measurement of tracer incorporation in liver TAG were not performed for obvious ethical reasons we cannot exclude the possibility that some newly synthesized fatty acids remained within liver TAG stores. However, it seems very unlikely that an increase in liver TAG stores
could explain a large part of the disposal of ingested glucose in study 2 and of the weight gain observed during the high energy high carbohydrate diet. An increase in lipogenesis in another tissue is unlikely. Therefore the most probable explanations for the observed body weight
increase are merely a repletion of muscles and liver glycogen stores, along with the simultaneous storage of water, and the suppression of fat oxidation leading to the deposition of ingested fat. Moreover, altough the contribution of fat to total energy intake was decreased during the high energy, high carbohydrate diet, the total amount ingested was increased.

In conclusion, our results show that in normal humans adipose tissue lipogenesis, although active, is quantitatively a minor pathway and is less responsive than hepatic lipogensis to acute or prolonged carbohydrate overfeeding. The picture could be different in obesity but the recent finding that lipogenic genes expression is decreased in adipose tissue of obese subjects (11) makes this possibility unprobable. Thus, DNL in adipose tissue is an unlikely contributor to the development of dietary induced obesity in humans.

I cannot upload the pdf, but if you would like a copy to read the whole article send me a PM. Also, if you would like a physiological explanation of carbohydrate metabolism and its effects on insulin and insulin dependent transporters send me a PM.

I would rather eat more protein than carbs. It works for me so I might as well keep doing it. My macros are about 50-25-25. I feel good eating like this. I ate this way while taking h-drol and bold and I gained a considerable amount of strength-and kept those gains after PCT. I only gained about 8 pounds. I would like to try a different compound this time around. I wish M-DHT were still around because that stuff made me very aggressive and strong., but didnt put any weight on me.

since no one here has your metabolism, work out routine, or diet we can only give suggestions or personal experiences... and i will give you the latter.... I have run a few (solo) SD cycle, (solo)2 h-drol cycles, and 1 epi cylce( few others and a few combos) but i will agree with alot of the former posts.... you will get great strength gains on sd..... h-drol is good... but i will give you both experiences on my sd cycles..... one for bulking and one for strength....... bulking cycle: i had a good heavy routine with around 4500-5000 cal per day 120g fat, 400 g protein, 500 g carbs.. gained 15.6 lbs after pct kept roughly 9.5lbs.... strength/cutting but not much cutting b/c its sd. 3500 calories a day 100g fat, 350g protein and 300 carbs... i know this is a rather low caloric intake but i got 7-10% gains off of the strength cycle. after pct i gained about a 1-2 lbs but thats just a good trip to the porcelain princess to break even... slightly alternated workout routine due to the ultimate goal...so for instance bench went from 300 to 330lbs... ect pretty solid gains but i did get a little more strength gains on the bulking cycle of sd when compared to the latter cycle...
take it what you will.. i am not as experienced in PH as alot of people here... i can only tell you what i have been though.

as a side note: when i am on no PH or ASS my usual caloric intake is roughly 2800-3000 cals a day... and that is to maintain body weight...

when weight comes on that fast, its not muscle. Its rapid uptake of water and glycogen puffing out the muscles. Its not keepable by itself, but it allows your muscles to work way harder and get way stronger, and its in the ensuing days that actual muscle is built. thought i should clarify that.

This is exactly what happens with creatine, but most people dont know that. They think the creatine is building the muscle but its not, it only allows you to lift a little bit heavier and train a little bit longer which in turn will make you grow faster.

This is exactly what happens with creatine, but most people dont know that. They think the creatine is building the muscle but its not, it only allows you to lift a little bit heavier and train a little bit longer which in turn will make you grow faster.

Indeed, creatine in short is broken down by creatine kinase to cleave its phosphate group to be used to synthesis ATP from ADP & AMP.

Now that all the Tren products are gone from the reputable websites to order from, I will have to stick with what I have anyway. I guess I can just run each product solo and with breaks and PCT it will last about a year.

In conclusion, the lipogenic capacity of adipose tissue is lower in humans than in rats. This is not related to differences in diet and is probably explained by lower abundance of SREBP-1c protein. A decreased expression of ChREBP could also play a role.

De novo lipogenesis did not differ significantly between lean and obese subjects, except with the control treatment, for which de novo lipogenesis was greater in the obese subjects. De novo lipogenesis was 2- to 3-fold higher after overfeeding by 50% than after the control treatment in all subjects. The type of carbohydrate overfeeding (sucrose or glucose) had no significant effect on de novo lipogenesis in either subject group. Estimated amounts of absolute VLDL production ranged from a minimum of 2 g/d (control) to a maximum of 10 g/d after overfeeding.

Wow. I understand the concept and have looked into it b4 but the part that caught me off guard was that the were taking in 150% of their BMR requirements. That is WAY more kcals than needed. I would have figured that given sufficent insulin (and seeing that the extra 50% was CHO, I'm sure there is), that would be enough kcals to increase adipose tissue significantly no matter what macro it was. I would like to know how they figured their BMR though. If just useing one of the many calculators, and not experimenting themselves to find their true BMR, theresults would be badly skewed. The formulas are usually quite a bit off. Does it say in the study if there is a controll group takeing 100% of their BMR useing the same formula to figure it?

Wow. I understand the concept and have looked into it b4 but the part that caught me off guard was that the were taking in 150% of their BMR requirements. That is WAY more kcals than needed. I would have figured that given sufficent insulin (and seeing that the extra 50% was CHO, I'm sure there is), that would be enough kcals to increase adipose tissue significantly no matter what macro it was. I would like to know how they figured their BMR though. If just useing one of the many calculators, and not experimenting themselves to find their true BMR, theresults would be badly skewed. The formulas are usually quite a bit off. Does it say in the study if there is a controll group takeing 100% of their BMR useing the same formula to figure it?

Exact BMR can be easily calculated through an open-circuit spirometry test. No use of a 'calculator'.